Signal transduction pathways, with multiple stimulators and multiple outcomes, have proven more complex than initially thought. Studying the regulation of pseudohyphal growth in yeast provides an opportunity to examine a set of interlocking pathways similar to those found in mammalian cells with the benefit of greater genetic and biochemical manipulations. It is accepted that RAS2, the Saccharomyces cerevisiae homologue of the protooncogene ras, and two RAS2-dependent pathways (a MAPK pathway and the adenylate cyclase pathway) are integral to the pseudohyphal growth response. However, these two pathways mediate responses other than the transition to pseudohyphal growth. How RAS2 interacts with these potentially parallel pathways to initiate pseudohyphal growth is unknown and the subject of this proposal. Specifically, we intend to (1) examine the interactions between RAS2 and its effectors and (2) conclusively establish a link between RAS2 and members of the MAPK module.